Genetic characterisation of the emerging invasive Neisseria meningitidis serogroup Y in Sweden, 2000 to 2010.

Genetic characterisation of the emerging invasive Neisseria meningitidis serogroup Y in Sweden, 2000 to 2010.
复制标题

2000 年至 2010 年瑞典新出现的侵袭性脑膜炎奈瑟菌 Y 血清群的遗传特征。

DOI:
--
复制
发表时间:
2011
期刊:
Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin
影响因子:
--
通讯作者:
P. Mölling
P. Mölling
中科院分区:
--
文献类型:
--
作者:
S. T. Hedberg;B. Törös;H. Fredlund;P. Olcén;P. Mölling

文献摘要

被引文献

相似文献

脑膜炎奈瑟菌血清群B和C是欧洲大多数侵袭性脑膜炎球菌病的原因。近年来,N.在瑞典(2010年,这一比例为39%,发病率为每100,000人0.23例)以及其他北方欧洲国家,都发现了由血清群Y引起的脑膜炎。我们的目的是调查2000年至2010年期间在瑞典出现的血清群Y的克隆模式。通过fetA、fHbp、佩纳、porA和porB基因的多位点序列分型和测序对在此期间鉴定的血清群Y分离株(n=85)进行表征。最常见的克隆(包括28个分离物)具有相同的等位基因组合的研究基因,是部分负责观察到的N。脑膜炎血清群Y分离株。它是磺胺嘧啶耐药的,基因亚型P1. 5 - 2,10 - 1,36 -2,序列类型23,克隆复合体23,porB等位基因3-36,fetA等位基因F4-1,fHbp等位基因25和佩纳等位基因22。2002年发现了第一例由该克隆引起的疾病:2004年又有一例,2006至2007年有6例,2008至2009年有8例,2010年最多有12例。由该克隆引起的年轻人(20-29岁)的侵袭性疾病异常增加,但没有观察到死亡率增加。
Neisseria meningitidis serogroups B and C have been responsible for the majority of invasive meningococcal disease in Europe. Recently, an increase of N. meningitidis disease due to serogroup Y has been noted in Sweden (in 2010, the proportion was 39%, with an incidence of 0.23 per 100,000 population), as well as in other northern European countries. We aimed to investigate the clonal pattern of the emerging serogroup Y in Sweden during 2000 to 2010. The serogroup Y isolates identified during this time (n=85) were characterised by multilocus sequence typing and sequencing of the fetA, fHbp, penA, porA and porB genes. The most frequent clone (comprising 28 isolates) with identical allele combinations of the investigated genes, was partly responsible for the observed increased number of N. meningitidis serogroup Y isolates. It was sulfadiazine resistant, with genosubtype P1.5-2,10-1,36-2, sequence type 23, clonal complex 23, porB allele 3-36, fetA allele F4-1, fHbp allele 25 and penA allele 22. The first case with disease due to this clone was identified in 2002: there was a further case in 2004, six during 2006 to 2007, eight during 2008 to 2009, with a peak of 12 cases in 2010. An unusual increase of invasive disease in young adults (aged 20–29 years) caused by this clone was shown, but no increase in mortality rate was observed.